Archives of Academic Emergency Medicine. 2022; 10(1): e78 REV I EW ART I C L E From Q/Non-Q Myocardial Infarction to STEMI/NSTEMI: Why It’s Time to Consider Another Simplified Dichotomy; a Narrative Literature Review Grigorios Avdikos1∗, George Michas2, Stephen W. Smith3 1. Department of Cardiology, Bioiatriki Healthcare Group, 132 Kifisias Ave. & Papada st., 11526, Athens, Greece. 2. Department of Cardiology, “Elpis” General Hospital of Athens, Dimitsanas 7, 11522, Athens, Greece. 3. Hennepin Healthcare, University of Minnesota School of Medicine, HCMC ER, R-2, 701 S. Park Ave., Minneapolis, MN 55415, United States of America. Received: July 2022; Accepted: August 2022; Published online: 1 October 2022 Abstract: Acute coronary syndromes (ACSs) are classified as ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) based on the presence of guideline-recommended ST-segment elevation (STE) criteria on the electrocardiogram (ECG). STEMI is associated with acute total coro- nary occlusion (ATO) and transmural myocardial necrosis and is managed with emergent reperfusion therapy, and NSTEMI is supposedly synonymous with subendocardial myocardial infarction without ATO. However, coronary angiograms reveal that a significant proportion of patients with NSTEMI have ATO. Here, we review articles that studied the frequency and cardiovascular outcomes of ATO in NSTEMI patients compared with those without ATO. We discuss ECG patterns of patients with suspected acute myocardial infarction that do not fulfill STEMI criteria but are associated with ATO. Under-recognition of these atypical patterns results in delays to reperfusion therapy. We also advocate revision of the current STEMI/NSTEMI paradigm because consider- ation of STE, by itself, out of context of other clinical and ECG features, leads to the ECG diagnosis of STEMI when the ECG actually represents a mimic [“Pseudo-STEMI”], and suggest renaming the ACSs classification as the Occlusion Myocardial Infarction (OMI)/Non-Occlusion Myocardial Infarction (NOMI) paradigm. Keywords: Acute coronary syndrome; coronary occlusion; myocardial infarction; myocardial reperfusion; non-ST elevated myocardial infarction Cite this article as: Avdikos G, Michas G, Smith SW. From Q/Non-Q Myocardial Infarction to STEMI/NSTEMI: Why It’s Time to Consider An- other Simplified Dichotomy; a Narrative Literature Review. Arch Acad Emerg Med. 2022; 10(1): e78. https://doi.org/10.22037/aaem.v10i1.1783. 1. Introduction Acute coronary syndromes (ACSs) remain a leading cause of morbidity and mortality worldwide. The 12-lead electrocar- diogram (ECG) is a valuable tool for early recognition of acute myocardial ischemia. The presence or absence of pathologic Q waves on the ECG formerly resulted in classification of acute myocardial infarction (AMI) as Q-wave or non-Q-wave myocardial infarction (MI). In 2000, the ACC/AHA guide- lines (1) announced a paradigm shift: patients presenting with ST-segment elevation (STE) on the ECG were grouped as having ST-segment elevation acute myocardial infarction ∗Corresponding Author: Grigorios Avdikos; Department of Cardiology, Bioiatriki Healthcare Group, 132 Kifisias Ave. & Papada st., 11526, Athens, Greece. Email: goranavdi@yahoo.gr, Tel: +306942906463, ORCID: https://orcid.org/0000-0002-1890-1646. (STEMI) and those without STE as non-ST-segment elevation myocardial infarction (NSTEMI). STEMI would purportedly represent acute total coronary occlusion (ATO) myocardial infarction (Occlusion MI or OMI) and NSTEMI would pur- portedly represent AMI without ATO (Non-Occlusion MI or NOMI). Prompt recognition of STE in the pre-hospital setting or in the Emergency Department by the paramedics and/or physicians is of great importance because the treatment of STEMI is urgent reperfusion with thrombolytics or primary coronary intervention. However, in reality, many patients who present with NSTEMI have ATO or subtotal occlusion on the coronary angiogram. A meta-analysis of seven stud- ies showed that 25.5% of NSTEMI patients had ATO with in- creased adverse short and medium to long term cardiovascu- lar outcomes, compared with NSTEMI patients without ATO (2). Furthermore, advances in ECG interpretation have re- vealed numerous high-risk ECG presentations without STE This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Downloaded from: http://journals.sbmu.ac.ir/aaem G. Avdikos et al. 2 that are associated with ATO for which early reperfusion ther- apy could be beneficial. The aim of the current narrative re- view is to study the frequency and cardiovascular outcomes of ATO in NSTEMI patients, provide a summary of ECG pat- terns without STE that are associated with ATO, and support a paradigm shift of the current STEMI/NSTEMI classification of ACS. 2. Methods We searched the electronic database of PubMed from in- ception up to 22 August 2022 for articles that studied: i) patients who underwent percutaneous coronary an- giogram/intervention (PCI) for NSTEMI, ii) the incidence (or prevalence) of ATO on the coronary angiogram of this pop- ulation, and iii) cardiovascular outcomes of patients with ATO compared with those without ATO. Exclusion criteria in- cluded non-English manuscripts, case reports and editorials. The following terms were used: (incidence OR prevalence OR frequency) AND (impact OR outcomes) AND (total artery oc- clusion OR culprit lesion) AND (NSTEMI OR non-ST eleva- tion myocardial infarction). The titles and abstracts were re- viewed, independently, by 2 authors (GA, GM) and unrelated studies were excluded. Full-text evaluation of the remain- ing articles was performed and studies that satisfied eligibil- ity criteria were included in the review. Disagreements be- tween reviewers were resolved after discussion with the third author (SS). Similar articles of the selected studies were also evaluated for eligibility. Figure 1 shows the flow diagram of the study. 3. Findings 3.1. Outcomes of NSTEMI cases with ATO We identified 192 records. Four observational studies and 2 meta-analyses were included in the present review. In a systematic review and meta-analysis (3) data from 25 stud- ies were analyzed, the average proportion of ATO in NSTEMI patients was 34% (95% CI 30%-37%). Death rate, recurrent MI and cardiogenic shock were significantly higher in ATO NSTEMI patients compared with those without ATO (OR: 1.72, 95% CI: 1.49-1.98, p < 0.001, OR 1.7: 95% CI: 1.06-2.75, p = 0.029 and OR: 1.66, 95% CI: 1.35-2.04, p < 0.001, respec- tively). Khan et al. (2) published a systematic review and meta-analysis of 7 studies and reported Thrombolysis in My- ocardial Infarction (TIMI) flow 0-1 in 25.5% of NSTEMI pa- tients. This group had increased short and medium-to long- term risk of major adverse cardiovascular events (MACE) (RR: 1.41, 95% CI: 1.17-1.70, p = 0.0003 and RR: 1.32, 95% CI: 1.11- 1.56, p = 0.001, respectively) and all-cause mortality (RR: 1.67, 95% CI: 1.31-2.13, p<0.0001 and RR: 1.42, 95% CI: 1.08-1.86, p=0.01, respectively). More recently, in a large Polish registry (4) the proportion of ATO with TIMI flow 0 was 19.9% among 81415 NSTEMI pa- tients and was associated with higher incidence of cardiac arrest before admission (3.09% vs. 2.19%, p<0.0001), Killip class IV on admission (2.48% vs. 1.69%, p<0.0001), death dur- ing PCI (0.97% vs. 0.43%, p<0.0001), and the lower frequency of TIMI flow 3 after PCI (83.36% vs. 88.61%, p<0.0001). Morawska et al. (5) found increased in-hospital and one- year mortality in NSTEMI patients presenting with ATO com- pared with NSTEMI patients with patent coronary arteries (2.8 % vs. 1.1%, p=0.007 and 18.1% vs. 6.5%, p<0.001, respec- tively). Another observational study (6) found statistically in- significant differences between ATO and non-ATO NSTEMI patients regarding in- hospital (5.3% vs. 1%, p=0.07) and 6- month MACE (5.4% vs. 4.6%, p=0.24). Fernando et al. (7) studied the long-term cardiovascular outcomes of occluded culprit arteries in NSTEMI patients and found lower rates of mortality in ATO NSTEMI patients when compared with NSTEMI patients without ATO with an average follow up of 4.9 years (12% vs. 18%, p<0.01), despite the increased 30-day MACE observed in this group (6.7% vs. 3.8%, p<0.001). Multi- variate analysis of this study showed that age, traditional car- diovascular risk factors, heart failure, renal impairment, and multivessel coronary artery disease are all independent pre- dictors of long-term mortality, whereas ATO was not. Thus, higher rates of long-term mortality in NSTEMI patients with- out ATO may be attributed to the greater prevalence of co- morbidities in this group. Table 1 shows published articles that studied the frequency of ATO and cardiovascular out- comes in NSTEMI patients compared with NSTEMI patients without ATO. Overall, approximately 25%-30% of patients presenting with NSTEMI have ATO with increased adverse short-term car- diovascular outcomes compared with NSTEMI patients with patent coronary arteries, with some discrepancies regarding long-term cardiovascular outcomes. 3.2. High-risk ECG patterns associated with ATO According to the fourth universal definition of MI, ECG cri- teria for STEMI diagnosis are STE ≥1 mm in two contiguous leads, except leads V2-V3 where the following cut-points ap- ply: ≥2 mm in men ≥40 years; ≥2.5 mm in men <40 years or ≥1.5 mm in women regardless of age (8). These current formal criteria are based on the modification of the 2000 ACC/ESC criteria by Macfarlane et al. (9) However, some pa- tients present with ECG patterns that are associated with ATO but do not fulfill the above-mentioned STEMI criteria. Below, we briefly discuss these ECG patterns. Acute myocardial infarction is a dynamic phenomenon and hyperacute T waves often precede STE. There is not a clear definition of hyperacute T waves, but they are often de- scribed as symmetric, tall, with high amplitude proportional This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Downloaded from: http://journals.sbmu.ac.ir/aaem 3 Archives of Academic Emergency Medicine. 2022; 10(1): e78 to the QRS and depend mainly on recognition rather than on criteria (10). An old study (11) found that a combination of J point/T wave amplitude >25%, T wave/QRS amplitude >75% and J point >0.30 mV in patients >45 years old predicts clini- cally verifiable MI with 98% specificity and 61.9% sensitivity. Many authors agree that T-wave height is not as important as T-wave “bulk,” defined as a proportion of the area under the curve of the T-wave to QRS size (10, 12, 13). Diagnosis of ACS in the presence of left bundle branch block (LBBB) can be challenging. Sgarbossa et al. (14) proposed a score composed of 3 criteria for the diagnosis of acute MI in patients presenting with LBBB; however, it has low sensitivity. More recently, Smith’s modified Sgarbossa criteria were pub- lished: STE ≥1mm concordant with QRS in any lead, or ST- segment depression (STD) ≥ 1mm in any of leads V1-V3, or excessively discordant STE with ST/S ratio ≥ 25% in any lead predicted Occlusion MI (OMI) in patients with LBBB (15). These criteria were validated in a study by Meyers et al. (16) and showed significantly higher sensitivity and similarly high specificity compared with the original Sgarbossa criteria. Us- ing a ST/S ratio criterion of 20% improves sensitivity to 84% and only reduces specificity to 94%. Right ventricular paced rhythm poses another diagnostic challenge. Dodd et al. (17) compared Smith’s modified Sgar- bossa criteria, which defines excessively discordant STE as an ST/S ratio of 25% (with extension of the second criterion of STD ≥1mm to leads V4-V6), with the original Sgarbossa criteria, which defines excessively discordant STE as 5 mm, and found that it has higher sensitivity with similarly high specificity in diagnosis of OMI. Interpretation of the ECG in the setting of acute chest pain and new-onset right bundle branch block (RBBB) should be done with much care, be- cause RBBB can mask subtle STE in leads V1-V3 due to sec- ondary repolarization changes resulting in the depression of ST-segment and T wave inversion. New RBBB, especially when combined with left anterior fascicular block, is asso- ciated with occlusion of proximal left anterior descending artery (LAD) and increased in-hospital mortality (18). Wellens’ syndrome (19, 20) is defined by a post-anginal pe- riod and ECG findings of preserved R-waves and an isoelec- tric or <1 mm J point elevation and biphasic T waves in leads V2-V3 (Pattern A) or deeply inverted and symmetric T waves in leads V2-V3 (Pattern B); the T wave changes in both types may extend to V1, V4, V5 and V6. Wellens’ syndrome is re- lated with critical stenosis of proximal LAD and impending MI, and is actually a post-reperfusion pattern: if an ECG had been recorded during pain, the ECG would have manifested acute occlusion. Other myocardial locations (inferior, lat- eral) manifest identical findings in the post-reperfusion state; in the posterior wall, it manifests as increased T-wave am- plitude in V2 (“Posterior Reperfusion T-waves; Wellens’ syn- drome of the posterior wall”) (21) . More recently, de Win- ter’s ECG pattern (22) was associated with proximal LAD oc- clusion: minimal STE in lead aVR and hyperacute T waves with upsloping STD in leads V1-V6. Left circumflex artery (LCx) is the culprit artery of isolated posterior MI. Horizon- tal STD of any amount, maximal in leads V1-V4 versus V5- V6, predicts acute posterior OMI (versus nonocclusive is- chemia) with 97% specificity (23) . Another ECG pattern seen in LCx total occlusion is the N wave sign, which is recognized as notch or deflection ≥2mm in the terminal QRS complex in leads II, III and aVF and/or leads I, aVL with continuous change of the notch ≥2mm in ≥2 leads in 24 hours and pro- longed QRS duration in these leads (24) . Aslanger’s pattern (25) is a high-risk ECG presentation connected with occlu- sion of LCx or right coronary artery (RCA) with at least one accompanying stable but critical stenosis in one of the non- infarct-related arteries. Diagnostic criteria are any STE in lead III, with reciprocal STD in aVL, but no STE in other infe- rior leads, STD in any of leads V4-V6 (but not in V2) with pos- itive T wave and ST in V1 higher than in V2. Critical stenosis of the left main coronary artery (LM) or severe 3-vessel dis- ease can present with diffuse STD >1mm in at least 6 leads plus STE in aVR and/or V1 (26) . Marti et al. (27) found that 18% of patients with ATO had subtle STE, defined as STE 0.1- 1mm; 86% of them had TIMI flow grade 0/1. Patients with subtle STE had longer delays to reperfusion and similar rates of deaths and reinfarction compared with those who fulfilled formal STEMI criteria. Reciprocal STD ≥0.5 mm was present in 68% of patients with subtle STEMI and more specific in 75% of patients with inferior infarctions. Table 2 summarizes the high-risk ECG patterns associated with ATO. 3.3. Differentiation of normal, baseline STE from STE due to OMI Very often physicians face difficulties in diagnosing STEMI because many patients have non-ischemic STE. Normal vari- ant STE (NV-STE) is sometimes referred to as “early repolar- ization,” even though this term has a more specific meaning. NV-STE may be present in anterior, lateral, or inferior leads. It is crucial to differentiate anterior STEMI from NV-STE ECG pattern in anterior leads in the setting of acute chest pain. Smith et al. (28) found a formula of 3 variables (STE 60ms af- ter J point in lead V3, QTc segment duration, and amplitude of R wave in lead V4) that predicted anterior STEMI with 86% sensitivity, 91% specificity and accuracy of 88%. After adding QRS voltage in lead V2, the accuracy of the 4-variable for- mula increased to 92% (29). These 2 formulas were externally validated and showed high sensitivity, specificity and diag- nostic accuracy (30). Moreover, presence of terminal QRS distortion (TQRSD = absence of both an S and J wave in ei- ther V2 or V3) is a useful ECG sign to differentiate anterior STEMI from NV-STE with 100% specificity (i.e., no case of NV-STE had TQRSD) (31). ECG presentation of left ventric- This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Downloaded from: http://journals.sbmu.ac.ir/aaem G. Avdikos et al. 4 ular aneurysm can mask acute critical occlusion of LAD. Cri- terion that supports the diagnosis of anterior STEMI is any V1-V4 T wave/QRS amplitude ≥0.36 (32, 33). Table 3 shows ECG patterns with normal, baseline STE and proposed crite- ria to differentiate STE due to OMI. 3.4. From Q/non-Q MI to STEMI/NSTEMI The previous paradigm of ACS (Q/non-Q MI) reflects the natural history of MI: treatment with antithrombotics with- out reperfusion cannot reverse ongoing myocardial necro- sis in the case of ATO and it ultimately leads to large ter- ritory complete infarction, with subsequent scarring. This phenomenon is expressed with Q wave on the ECG. The Fib- rinolytic Therapy Trialists’ (FTT) Collaborative Group, pub- lished in 1994 a landmark systematic review of 9 random- ized trials, which studied the effect of fibrinolytic therapy in suspected acute MI (34). They concluded that throm- bolysis was associated with reduction in mortality and this benefit was observed mainly among patients presenting with STE or bundle branch block (BBB) and when therapy was re- ceived up to 12 hours from symptom onset. However, en- rollment criteria were “suspected MI”; 4/9 studies required STE but poorly defined; 5/9 had no required ECG findings; 38% of patients were enrolled after at least 6 hours of chest pain, when treatment is much less effective, and 7/9 stud- ies used the less effective streptokinase (35-43). For example, in the second International Study of Infarct Survival (ISIS-2) (37) and the Anglo-Scandinavian Study of Early Thromboly- sis (ASSET) (43) trials patients with clinically suspected acute MI and without specific ECG changes (including unspecified STE, BBB, STD or normal ECG) were included and in other studies (35, 39) patients with STE ≥1mm in limb leads or ≥2mm in chest leads were deemed eligible, these cut-offs dif- fer from those recommended in the fourth universal defini- tion of MI for STEMI diagnosis. STE and STD were also ret- rospectively classified. Based on this data, they concluded that STE is the best way to decide on thrombolytic therapy (no placebo-controlled trial of mechanical intervention has ever been done). But this is only true if ECG interpretation is crude, patients are treated after 6 hours, and streptokinase is used (not PCI). But what about less obvious STE, hyperacute T-waves, ST-T morphology, terminal QRS distortion, propor- tionality between QRS and ST-T, associated Q-waves, etc.? Since no coronary angiograms were performed, an unknown number of patients with ECG presentations like normal ECG, pre-existing BBB, acute pericarditis, acute myocarditis, hy- perkalemia, “early repolarization”, and left ventricular hyper- trophy received fibrinolytic therapy without actually having acute MI. Furthermore, according to the authors, it was un- clear whether fibrinolytic therapy benefits patients present- ing with STD or other ECG abnormalities but without STE or BBB and they mentioned that the number of deaths among such patients was relatively small. Due to the results of the FTT Collaborative Group systematic review, classification of ACS changed officially from Q/non-Q MI to STEMI/NSTEMI in the 2000 ACC/AHA guidelines. 3.5. STEMI/NSTEMI paradigm in the era of me- chanical reperfusion According to the European guidelines (44), therapy of STEMI is immediate reperfusion with thrombolysis or PCI, and anal- ogous treatment (invasive therapy <2h from hospital ad- mission) should be administered to NSTEMI patients with mechanical complications, cardiogenic shock, refractory angina, life-threatening arrhythmias, and acute heart failure (26). In spite of these NSTEMI guidelines, very few (6.4%) such patients are actually taken for angiography within 2 hours (45). Early recognition of STE in the setting of acute chest pain is a critical initial step in the management of ACS. However, not all STE are due to acute MI: acute pericardi- tis, “early repolarization”, left ventricular hypertrophy and aneurysm, takotsubo cardiomyopathy, and hyperkalemia are some examples that present with STE on the ECG. It was found that 15%-36% (46, 47) of catheter laboratory activa- tions due to perceived STEMI were false positive without culprit lesion on the coronary angiogram. Major dilemmas emerge in non-PCI-capable centers and time to PCI >120 min, where thrombolysis is the only option for urgent reper- fusion of STEMI and false diagnosis could be catastrophic due to possible serious hemorrhagic complications. On the other hand, as we discussed earlier in the present review, not all acute MI with proven ATO present with STE and a number of such high-risk ECG patterns can be recognized (the so-called STEMI equivalents). In addition, about 25%- 30% of NSTEMI patients have ATO with increased adverse cardiovascular outcomes compared with those with patent coronary arteries. Strict application of STEMI criteria in clinical practice excludes patients with de Winter’s pattern from receiving immediate reperfusion therapy and activates catheter laboratory for patients presenting with “early repo- larization” (Figure 2). A “holistic” ECG approach is needed: ECG interpretation in the clinical context of acute chest pain indicative of myocardial ischemia should not focus only on ST segment nor on whether any specific millimeter-based STE criteria are satisfied. In addition, ST and T wave should always be assessed in proportion to QRS. 3.6. What’s new in the European guidelines? In 2017, the ESC guidelines for STEMI (44) in addition to the new LBBB and the isolated posterior infarction, consid- ered two more atypical ECG presentations as high risk, which should prompt a primary coronary intervention strategy in patients presenting with ongoing symptoms consistent with myocardial ischemia: RBBB and diffuse STD ≥1 mm in at This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Downloaded from: http://journals.sbmu.ac.ir/aaem 5 Archives of Academic Emergency Medicine. 2022; 10(1): e78 least 8 leads coupled with STE in aVR and/or V1. The for- mer pattern suggests proximal critical LAD occlusion with poor prognosis and the latter points to ischemia due to left main coronary artery critical stenosis or severe multivessel disease. According to the latest ESC guidelines for NSTEMI in 2020 (26), those presenting with STD>1 mm in at least 6 leads plus STE in aVR and/or V1 are also considered very high-risk patients who should be managed with immediate (<2 hours) invasive strategy. Furthermore, in the supplemen- tary data, de Winter’s and Wellens’ patterns are mentioned as high-risk ECG presentations without STE associated with proximal LAD occlusion. There are many other subtle pat- terns of occlusion, which are more difficult to describe and teach. In their study (48), showing that expert ECG interpre- tation has equal specificity to the STEMI criteria and is more than twice sensitive in detection of OMI, Meyers et al. found the 7 patterns shown in Table 4. 3.7. The OMI/NOMI paradigm Many authors express concerns about the clinical perfor- mance of STEMI/NSTEMI classification of ACS (49-52). Mis- interpretation of STEMI mimics as STEMI, false positive catheter laboratory activations, under-recognition of high- risk ECG patterns without STE, proper risk stratification of NSTEMI patients, delays to reperfusion therapy, and dis- agreements between emergency physicians and interven- tional cardiologists are common problems. The main goal in the management of patients presenting with suspected acute MI is to provide immediate reperfusion therapy to those with ATO. Thus, the question that should be answered is whether the patient presenting to the emergency department with chest pain has an ECG indicative of ATO and not if pre- specified STE criteria are fulfilled. Based on this principle, Meyers, Weingart and Smith pro- posed the OMI/NOMI research classification of ACS (53). Oc- clusion Myocardial Infarction (OMI) is defined as an acute culprit coronary artery and either 1) TIMI flow 0-2 or 2) TIMI flow 3 plus 4th generation troponin T ≥ 1.0 ng/ml or I ≥10.0 ng/ml (5th generation, high sensitivity troponin, would be in ng/L and multiply by 1000) (48). OMI refers to type 1 acute coronary syndrome involving acute occlusion or near occlusion of a major epicardial coronary vessel with insuf- ficient collateral circulation, resulting in imminent necro- sis of downstream myocardium without emergent reperfu- sion. OMI is the anatomic and pathophysiologic substrate of STEMI, but not all OMI manifest as STEMI. Non-occlusion Myocardial Infarction (NOMI) refers to acute MI without an- giographic, laboratory or clinical evidence of OMI (NSTEMI without ATO). The term OMI includes STEMI patients who fulfill the current STEMI criteria [STEMI (+) OMI] and those who do not meet these criteria [STEMI (-) OMI or NSTEMI with ATO]. OMI requires emergent reperfusion therapy be- cause of ATO. The DIagnostic accuracy oF electrocardiogram for acute coronary OCClUsion resuLTing in myocardial in- farction (DIFOCCULT) study (54) found that the OMI/NOMI approach to ECG interpretation had superior diagnostic ac- curacy compared with the STEMI/NSTEMI approach in pre- diction of ATO and long-term mortality. Meyers et al. (48) showed that STEMI (-) OMI (NSTEMI with ATO) patients had significant delays to catheterization but adverse out- comes more similar to STEMI (+) OMI. More importantly, they found that expert ECG interpretation had sensitivity of 86% for diagnosis of OMI (vs. 41% for STEMI criteria) with specificity equal to STEMI criteria. Before the era of reperfusion therapy, anti-thrombotics (mainly aspirin and heparin) were used for the treatment of ACS. In the case of a total occluded coronary artery, trans- mural myocardial necrosis could not be reversed and Q wave was recorded on the ECG. This Q/non-Q paradigm was re- placed by the STEMI/NSTEMI dichotomy based on the re- duced mortality of patients who presented with suspected acute MI and STE who received thrombolytic therapy. Since then, STE is considered as a surrogate of ATO. However, coro- nary angiograms revealed that not all ECG presentations with STE are due to ATO and that a number of ECG patterns with- out STE are associated with ATO. This relation is expressed by the OMI/NOMI paradigm. Figure 3 shows a proposed evo- lution of ACS classification. One final thought: what other pathology has been named for a test? STEMI is named for one very imperfect aspect of one test (STE on the ECG). The pathology should be named for what it is: Occlusion MI. Its diagnosis can usually be made by expert ECG interpretation, but it is important to know that many OMIs do not manifest on the ECG, that many which do manifest on the ECG are not accurately interpreted by providers, and that one must of- ten use modalities other than the ECG to make the diagnosis, including emergent echocardiogram, CT coronary angiogra- phy, or angiogram itself. For acute symptoms, initial (and es- pecially 1- or 2-hour) troponin concentration is more likely to be less than the 99th percentile and the delay to reperfusion is too long (55). 4. Conclusion Recent studies suggest that 25%-30% of NSTEMI patients have ATO with increased adverse cardiovascular outcomes compared with those with patent coronary arteries. Early recognition of this high-risk group of ACS patients is based on the identification of ECG patterns that are related to ATO and do not satisfy current STEMI criteria. Knowledge and con- tinuous training in interpretation of these ECG presentations could improve management and outcomes of ACS patients. Considering STE as a hallmark of acute MI with ATO can be at times misleading and STEMI/NSTEMI classification should This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Downloaded from: http://journals.sbmu.ac.ir/aaem G. Avdikos et al. 6 be revised to include more high-risk ECG patterns that signify ATO. We agree with renaming the paradigm as the Occlusion MI/Non-Occlusion MI paradigm. 5. Declarations 5.1. Acknowledgments None. 5.2. Authors’ contributions G.A. and G.M. wrote the manuscript, and searched and ana- lyzed the data. S.S. wrote and revised the article. All authors read and approved the final version of manuscript. 5.3. Funding None. 5.4. Conflict of interest The authors declare that they have no competing interests. References 1. Braunwald E, Antman EM, Beasley JW, Califf RM, Cheitlin MD, Hochman JS, et al. ACC/AHA guidelines for the man- agement of patients with unstable angina and non-ST- segment elevation myocardial infarction: executive sum- mary and recommendations. A report of the American College of Cardiology/American Heart Association task force on practice guidelines (committee on the man- agement of patients with unstable angina). Circulation. 2000;102(10):1193-209. doi: 10.1161/01.cir.102.10.1193. PubMed PMID: 10973852. 2. Khan AR, Golwala H, Tripathi A, Bin Abdulhak AA, Bav- ishi C, Riaz H, et al. Impact of total occlusion of cul- prit artery in acute non-ST elevation myocardial infarc- tion: a systematic review and meta-analysis. Eur Heart J. 2017;38(41):3082-9. 3. Hung C-S, Chen Y-H, Huang C-C, Lin M-S, Yeh C-F, Li H- Y, et al. Prevalence and outcome of patients with non-ST segment elevation myocardial infarction with occluded “culprit” artery–a systemic review and meta-analysis. Crit Care 2018;22(1):1-11. 4. Terlecki M, Wojciechowska W, Dudek D, Siudak Z, Plens K, Guzik TJ, et al. Impact of acute total occlusion of the culprit artery on outcome in NSTEMI based on the re- sults of a large national registry. BMC Cardiovasc. Disord. 2021;21(1):1-9. 5. Morawska I, Niemiec R, Stec M, Wrona K, Bańka P, Swinarew A, et al. Total Occlusion of the Infarct- Related Artery in Non-ST-Elevation Myocardial Infarc- tion (NSTEMI)—How Can We Identify These Patients? Medicina. 2021;57(11):1196. 6. Ayad SW, El Zawawy TH, Lotfy MI, Naguib AM, El Am- rawy AM. Incidence and impact of totally occluded cul- prit coronary artery in patients with non-ST segment el- evation myocardial infarction acute coronary syndrome. Egypt Heart J. 2021;73(1):1-9. 7. Fernando H, Duffy SJ, Low A, Dinh D, Adrianopoulos N, Sharma A, et al. Totally Occluded Culprit Coronary Artery in Patients with Non-ST-Elevation Myocardial Infarction Undergoing Percutaneous Coronary Intervention. Am J Cardiol. 2021;156:52-7. 8. Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Mor- row DA, et al. Fourth universal definition of myocardial infarction (2018). J Am Coll Cardiol. 2018;72(18):2231-64. 9. Macfarlane PW, Browne D, Devine B, Clark E, Miller E, Seyal J, et al. Modification of ACC/ESC criteria for acute myocardial infarction. J Electrocardiol. 2004;37:98-103. 10. Miranda DF, Lobo AS, Walsh B, Sandoval Y, Smith SW. New insights into the use of the 12-lead electrocardio- gram for diagnosing acute myocardial infarction in the emergency department. Can J Cardiol. 2018;34(2):132- 45. 11. Collins MS, Carter JE, Dougherty JM, Majercik SM, Hods- den JE, Logue EE. Hyperacute T-wave criteria using com- puter ECG analysis. Ann Emerg Med. 1990;19(2):114-20. 12. Aslanger EK, Meyers HP, Smith SW. Recognizing electro- cardiographically subtle occlusion myocardial infarction and differentiating it from mimics: Ten steps to or away from cath lab. Turk Kardiyol Dern Ars. 2021;49(6):488. 13. Smith SW. Dr Smith’s ECG Blog http://hqmeded- ecgblogspotcom [Internet]. [cited 22 August 2022]. 14. Sgarbossa EB, Pinski SL, Barbagelata A, Underwood DA, Gates KB, Topol EJ, et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. N Engl J Med. 1996;334(8):481- 7. 15. Smith SW, Dodd KW, Henry TD, Dvorak DM, Pearce LA. Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST- elevation to S-wave ratio in a modified Sgarbossa rule. Ann Emerg Med. 2012;60(6):766-76. 16. Meyers HP, Limkakeng Jr AT, Jaffa EJ, Patel A, Theiling BJ, Rezaie SR, et al. Validation of the modified Sgarbossa cri- teria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study. Am Heart J. 2015;170(6):1255-64. 17. Dodd KW, Zvosec DL, Hart MA, Glass III G, Bannister LE, Body RM, et al. Electrocardiographic diagnosis of acute coronary occlusion myocardial infarction in ventricular paced rhythm using the modified Sgarbossa criteria. Ann Emerg Med. 2021;78(4):517-29. 18. Widimsky P, Roháč F, Štásek J, Kala P, Rokyta R, Kuzmanov B, et al. Primary angioplasty in acute myocardial infarc- This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Downloaded from: http://journals.sbmu.ac.ir/aaem 7 Archives of Academic Emergency Medicine. 2022; 10(1): e78 tion with right bundle branch block: should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy? Eur Heart J. 2012;33(1):86-95. 19. De Zwaan C, Bär FW, Wellens HJ. Characteristic electro- cardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982;103(4):730-6. 20. Haines DE, Raabe DS, Gundel WD, Frans JT. Anatomic and prognostic significance of new T-wave inversion in unstable angina. Am J Cardiol. 1983;52(1):14-8. 21. Driver BE, Shroff GR, Smith SW. Posterior reperfusion T- waves: Wellens’ syndrome of the posterior wall. Emerg Med J. 2017;34(2):119-23. 22. de Winter RJ, Verouden NJ, Wellens HJ, Wilde AA. A new ECG sign of proximal LAD occlusion. N Engl J Med. 2008;359(19):2071-3. 23. Meyers HP, Bracey A, Lee D, Lichtenheld A, Li WJ, Singer DD, et al. Ischemic ST-Segment Depression Maximal in V1–V4 (Versus V5–V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia). J Am Heart Assoc. 2021;10(23):e022866. 24. Niu T, Fu P, Jia C, Dong Y, Liang C, Cao Q, et al. The de- layed activation wave in non-ST-elevation myocardial in- farction. Int J Cardiol. 2013;162(2):107-11. 25. Aslanger E, Yıldırımtürk Ö, Şimşek B, Sungur A, Cabbar AT, Bozbeyoğlu E, et al. A new electrocardiographic pat- tern indicating inferior myocardial infarction. J Electro- cardiol. 2020;61:41-6. 26. Collet J-P, Thiele H, Barbato E, Barthélémy O, Bauersachs J, Bhatt DL, et al. ESC Scientific Document Group. 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST- segment elevation. Eur Heart J. 2021;42(14):1289-367. 27. Martí D, Mestre JL, Salido L, Esteban MJ, Casas E, Pey J, et al. Incidence, angiographic features and outcomes of patients presenting with subtle ST-elevation myocardial infarction. Am Heart J. 2014;168(6):884-90. 28. Smith SW, Khalil A, Henry TD, Rosas M, Chang RJ, Heller K, et al. Electrocardiographic differentiation of early re- polarization from subtle anterior ST-segment elevation myocardial infarction. Ann Emerg Med. 2012;60(1):45- 56. e2. 29. Driver BE, Khalil A, Henry T, Kazmi F, Adil A, Smith SW. A new 4-variable formula to differentiate normal vari- ant ST segment elevation in V2-V4 (early repolarization) from subtle left anterior descending coronary occlusion- Adding QRS amplitude of V2 improves the model. J Elec- trocardiol. 2017;50(5):561-9. 30. Bozbeyoğlu E, Aslanger E, Yıldırımtürk Ö, Şimşek B, Karabay CY, Şimşek MA, et al. A tale of two formu- las: Differentiation of subtle anterior MI from benign ST segment elevation. Ann Noninvasive Electrocardiol. 2018;23(6):e12568. 31. Lee DH, Walsh B, Smith SW. Terminal QRS distortion is present in anterior myocardial infarction but absent in early repolarization. Am J Emerg Med. 2016;34(11):2182- 5. 32. Klein LR, Shroff GR, Beeman W, Smith SW. Electrocar- diographic criteria to differentiate acute anterior ST- elevation myocardial infarction from left ventricular aneurysm. Am J Emerg Med. 2015;33(6):786-90. 33. Smith SW. T/QRS ratio best distinguishes ventricular aneurysm from anterior myocardial infarction. Am J Emerg Med. 2005;23(3):279-87. 34. Trialists FT. Indications for fibronolytic therapy in sus- pected acute myocardial infarction: Collaborative trials of more than 1000 patients. Lancet. 1994;343(8893):311- 22. 35. ISAM Study Group. A prospective trial of intravenous streptokinase in acute myocardial infarction (ISAM). N Engl J Med. 1986;314(23):1465-71. 36. AIMS Trial Study Group. Effect of intravenous APSAC on mortality after acute myocardial infarction: prelimi- nary report of a placebo-controlled clinical trial. Lancet. 1988;331(8585):545-9. 37. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Randomized trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. J Am Coll Cardiol. 1988;12(6SA):A3-A13. 38. LATE Study Group. Late Assessment of Thrombolytic Efficacy (LATE) study with alteplase 6-24 hours af- ter onset of acute myocardial infarction. Lancet. 1993;342(8874):759-66. 39. Della DI, Miocardico SN. Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet. 1986;1(8478):397-402. 40. Hunt D, Varigos J, Dienstl F, Lechleitner P, De Backer G, KORNITZER M, et al. ISIS-3: a randomised comparison of streptokinase vs tissue plasminogen activator vs an- tistreplase and of aspirin plus heparin vs aspirin along among 41 299 cases of suspected acute myocardial in- farction. Lancet. 1992;339(8796):753-70. 41. Paolasso E, Ravizzini G. Randomized trial of late throm- bolysis in patients with suspected acute myocardial in- farction. Lancet. 1993;342(8874):767-72. 42. Rossi P, Bolognese L. Comparison of intravenous uroki- nase plus heparin versus heparin alone in acute myocar- dial infarction. Am J Cardiol. 1991;68(6):585-92. 43. Wilcox R, Olsson C, Skene A, Von Der Lippe G, Jensen G, Hampton J, et al. Trial of tissue plasminogen activa- tor for mortality reduction in acute myocardial infarc- This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Downloaded from: http://journals.sbmu.ac.ir/aaem G. Avdikos et al. 8 tion: Anglo-Scandinavian Study of Early Thrombolysis (ASSET). Lancet. 1988;332(8610):525-30. 44. Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli- Ducci C, Bueno H, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J. 2018;39(2):119-77. 45. Lupu L, Taha L, Banai A, Shmueli H, Borohovitz A, Matet- zky S, et al. Immediate and early percutaneous coronary intervention in very high-risk and high-risk non-ST seg- ment elevation myocardial infarction patients. Clin Car- diol. 2022;45(4):359-69. 46. Kontos MC, Kurz MC, Roberts CS, Joyner SE, Kreisa L, Or- nato JP, et al. An evaluation of the accuracy of emergency physician activation of the cardiac catheterization labo- ratory for patients with suspected ST-segment elevation myocardial infarction. Ann Emerg Med. 2010;55(5):423- 30. 47. McCabe JM, Armstrong EJ, Kulkarni A, Hoffmayer KS, Bhave PD, Garg S, et al. Prevalence and factors associated with false-positive ST-segment elevation myocardial in- farction diagnoses at primary percutaneous coronary in- tervention–capable centers: a report from the Activate- SF registry. Arch Intern Med. 2012;172(11):864-71. 48. Meyers HP, Bracey A, Lee D, Lichtenheld A, Li WJ, Singer DD, et al. Accuracy of OMI ECG findings ver- sus STEMI criteria for diagnosis of acute coronary oc- clusion myocardial infarction. Int J Cardiol Heart Vasc. 2021;33:100767. 49. Aslanger EK, Meyers HP, Smith SW. Time for a new paradigm shift in myocardial infarction. Anatol J Cardiol. 2021;25(3):156. 50. Phibbs B, Nelson W. Differential classification of acute myocardial infarction into ST-and non-ST segment ele- vation is not valid or rational. Ann Noninvasive Electro- cardiol. 2010;15(3):191-9. 51. Tziakas D, Chalikias G, Al-Lamee R, Kaski JC. Total coronary occlusion in non ST elevation myocardial in- farction: Time to change our practice? Int J Cardiol. 2021;329:1-8. 52. Widimský P, Rokyta R, Št J, Bělohlávek J, Červinka P, Kala P, et al. Acute coronary syndromes with ongoing my- ocardial ischemia (ACS with OMI) versus acute coro- nary syndromes without ongoing ischemia (ACS with- out OMI): The new classification of acute coronary syn- dromes should replace old classification based on ST segment elevation presence or absence—Expert consen- sus statement of the Czech Society of Cardiology. Cor Vasa. 2013;55(3):e225-e7. 53. Meyers HP, Weingart SD, Smith SW. The OMI Manifesto Dr Smith’s ECG Blog Available from: http://hqmeded- ecgblogspotcom/2018/04/the-omi-manifestohtml [Internet]. [cited 22 August 2022]. 54. Aslanger EK, Yıldırımtürk Ö, Şimşek B, Bozbeyoğlu E, Şimşek MA, Karabay CY, et al. DIagnostic accuracy oF electrocardiogram for acute coronary OCClUsion resuLT- ing in myocardial infarction (DIFOCCULT Study). Int J Cardiol Heart Vasc. 2020;30:100603. 55. Wereski R, Chapman AR, Lee KK, Smith SW, Lowe DJ, Gray A, et al. High-sensitivity cardiac troponin concentrations at presentation in patients with ST- segment elevation myocardial infarction. JAMA Cardiol. 2020;5(11):1302-4. This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Downloaded from: http://journals.sbmu.ac.ir/aaem 9 Archives of Academic Emergency Medicine. 2022; 10(1): e78 Table 1: Studies showing the frequency of acute total coronary occlusion (ATO) and cardiovascular outcomes in non-ST-segment elevation myocardial infarction (NSTEMI) patients compared with NSTEMI patients without ATO Study Year ATO definition (TIMI flow grade) Frequency of ATO in NSTEMI Cardiovascular outcomes (ATO vs. non-ATO) Morawska et al. (5)- observational study 2021 0 34.6% (138/399) -in-hospital mortality: (2.8% vs. 1.1%, p=0.007) -1-year mortality: (18.1% vs. 6.5%, p<0.001) Fernando et al. (7)- observational study 2021 0 14% (954/6829) -30-day MACE: (6.7% vs. 3.8%, p<0.001) -4.9-years mortality: (12% vs. 18%, p<0.01) Terlecki et al. (4)- observational study 2021 0 19.9% (16209/81415) -C.A. before admission (3.09% vs. 2.19%, P<0.0001) -Killip IV on admission: (2.48% vs. 1.69%, p<0.0001) -death during PCI: (0.97% vs. 0.43%, p<0.0001) -TIMI flow 3 after PCI: (83.36% vs. 88.61%, p<0.0001) Ayad et al. (6)- observational study 2021 0 22.4% (112/500) -in-hospital MACCE: (5.3% vs. 1%, p=0.07) -6-month MACCE: (5.4% vs. 4.6%, p=0.24) Hung et al. (3)-meta- analysis 2018 -in 21 studies: 0-1 -in 3 studies: 0 -in 1 study: 0-2 34% (95% CI 30%-37%) average proportion -death rate: (OR 1.72, 95% CI 1.49-1.98, p<0.001) -recurrent MI: (OR 1.7, 95% CI 1.06-2.75, p=0.029) -cardiogenic shock: (OR 1.66, 95% CI 1.35-2.04, p<0.001) Khan et al. (2)-meta- analysis 2017 0-1 25.5% (10415/40777) -short-term MACE: (RR 1.41, CI 1.17-1.70, p=0.0003) -medium- to long-term MACE: (RR 1.32, CI 1.11-1.56, p=0.001) -short-term all-cause mortality: (RR 1.67, CI 1.31-2.13, p<0.0001) -medium- to long-term all-cause mortality: (RR 1.42, CI 1.08-1.86, p=0.01) CI: confidence interval; TIMI: Thrombolysis in Myocardial Infarction, MACE: major adverse cardiac events, C.A: cardiac arrest, PCI: percutaneous intervention, MACCE: major adverse cardiac and cerebrovascular events, MI: myocardial infarction; OR: odds ratio; RR: relative risk. This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Downloaded from: http://journals.sbmu.ac.ir/aaem G. Avdikos et al. 10 Table 2: High risk electrocardiogram (ECG) patterns associated with acute total coronary occlusion (ATO) High risk ECG pat- tern Criteria for diagnosis of ATO Sensitivity/specificity Culprit artery Hyperacute T waves (10, 12, 13) - “Bulky”, fat, wide, and often also tall and symmetric T-waves, such that the area under the curve, compared to the QRS amplitude, is large -a combination of: •J point/T wave > 25% •T wave/QRS > 75% •J point > 0.30 mv and •age > 45 years old 61.9%/98% LAD, LCx or RCA Lbbb (15, 16) -Smith’s modified Sgarbossa criteria: •STE ≥1 mm concordant with QRS in any lead or •STD≥1 mm in any of V1-V3 or •STE/S wave ≥ 25% in any lead 80%/99% LAD, LCx or RCA RV paced rhythm (17) -Smith’s modified Sgarbossa criteria: •STE ≥1 mm concordant with QRS or •STD≥1mm in any of V1-V6 or •STE/S wave ≥ 25% in any lead 86%/83% LAD, LCx or RCA New RBBB ± LAH (18) - RBBB diagnostic criteria -Any STE is suspicious proximal LAD De Winter’s pattern (22) - 1-2 mm STE in aVR and: •hyperacute T waves in V1-V6 •upsloping STD 1-3 mm in V1-V6 proximal LAD Wellens’ syndrome (19, 20) -isoelectric or < 1mm elevated J point in a post-anginal period plus: •biphasic T waves in V2-V3 (Pattern A) or •deeply inverted and symmetric T waves in V2-V3 (Pattern B) •T wave changes may extend to V1, V4, V5, V6 69%/89% proximal LAD Diffuse STD (26) -STD > 1mm in ≥ 6 leads and: •STE in aVR and/or V1 LM or severe 3 vessel disease Aslanger’s pattern (25) -any STE in III, but not in other inferior leads, with reciprocal STD in aVL plus: •STD in any of V4-V6 but not in V2 with positive T wave •STE in V1 higher than in V2 LCx or RCA and 2 or 3 vessel disease N wave sign (24) -notch or deflection in the terminal QRS complex ≥2 mm in II, III and aVF and/or I, aVL plus •continuous change of the notch ≥2 mm in ≥ 2 leads in 24 hours •prolonged QRS in these leads 77%/89% and 53%/97% / or 64%/96% LCx Acute posterior OMI (23) -STD of any amplitude maximal in leads V1-V4 versus V5-V6 37.4%/97.6% LCx Subtle STEMI (27) -STE 0.1-1 mm combined with reciprocal STD ≥0.5 mm LCx, RCA or LAD LAD: left anterior descending artery, LCx: left circumflex artery, RCA: right coronary artery, LBBB: left bundle branch block, STE: ST-segment elevation, STD: ST-segment depression, RV: right ventricular, RBBB: right bundle branch block, LAH: left anterior hemiblock, LM: left main coronary artery, OMI: occlusion myocardial infarction; STEMI: ST-segment elevation myocardial infarction; aVR: augmented Vector Right; aVL: augmented Vector Left. Table 3: Electrocardiogram (ECG)patterns with normal, baseline ST-segment elevation (STE) and proposed criteria to differentiate STE due to Occlusion Myocardial Infraction (OMI)) ECG pattern Criteria for diagnosis of ATO Sensitivity/specificity Culprit artery NV-STE (“early repolarization”) -4-variable formula: •0.052xQTc – 0.151xQRSV2-0.268xRV4 + 1.062xSTE60V3 ≥ 18.2 88.8%/94.7% LAD (10, 29, 31) -terminal QRS distortion: •absence of both an S and J wave in either V2 or V3 20%/100% left ventricular aneurysm (32, 33) -any V1-V4 T /QRS ≥ 0.36 91.5%/81.3% LAD ATO: acute total coronary occlusion; NV-STE: normal variant ST-elevation; QTc: Bazett-corrected QT segment; QRSV2: QRS voltage in lead V2, RV4: R wave amplitude in lead V4; STE60V3: ST-segment elevation in lead V3 60ms after J point; LAD: left anterior descending artery. This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Downloaded from: http://journals.sbmu.ac.ir/aaem 11 Archives of Academic Emergency Medicine. 2022; 10(1): e78 Table 4: Frequency of 7 findings among 146 patients with Occlusion Myocardial Infarction (OMI), identified by expert earlier than by crite- ria/angiogram Feature Frequency Hyperacute T waves 49% Pathologic Q waves, along with subtle STE 47% Terminal QRS distortion 53% Reciprocal STD and/or Reciprocal T-wave inversion 82% Subtle STE not meeting criteria, but with other features 83% Any amount of STD maximal in V1-V4 45% Any STE in inferior leads with any STD/T-wave inversion in aVL 50% STE: ST-segment elevation; STD: ST-segment depression; aVL: augmented Vector Left. Figure 1: Flow diagram of the study. This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Downloaded from: http://journals.sbmu.ac.ir/aaem G. Avdikos et al. 12 Figure 2: Electrocardiogram (ECG) recordings from two male patients in their early 30s presenting with acute chest pain. ECG (A) is from a patient with de Winter’s pattern and ECG (B) is consistent with “early repolarization”. ECG (A) does not meet STEMI criteria but catheter laboratory was activated emergently and a total occluded left anterior descending artery was identified on the coronary angiogram and was stented successfully. ECG (B) satisfies current STEMI criteria but emergent treatment was not required. Serial unchanged ECG recordings with normal values of troponin and normal echocardiogram ruled out acute coronary syndrome. ECG (A) is reproduced after permission from Dr. Smith’s ECG blog. Available from: https://hqmeded-ecg.blogspot.com/2021/03/de-winters-t-waves-are-not-stable-ecg.html, courtesy of Stephen W. Smith, MD. Figure 3: Proposed evolution of acute coronary syndrome classifications. MI: Myocardial Infarction. This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Downloaded from: http://journals.sbmu.ac.ir/aaem Introduction Methods Findings Conclusion Declarations References